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Jun Luo

Publications and source records attributed to Jun Luo.

65 records · Page 4Linked to original sources
PubMed2002

Controlled mechanical ventilation leads to remodeling of the rat diaphragm.

Little is known about the structural response of the diaphragm to controlled mechanical ventilation. We examined effects of this intervention on muscle mass, myosin heavy chain isoforms, and contractile function in the rat diaphragm. Animals were mechanically ventilated for up to 4 days, and comparisons were made with normal control rats as well as spontaneously breathing animals anesthetized for the same duration as the mechanical ventilation group. The diaphragm-to-body weight ratio was significantly reduced in the mechanical ventilation group only. After mechanical ventilation, an increase in hybrid fibers coexpressing both type I (slow) and type II (fast) myosin isoforms was found within the diaphragm, which occurred at the expense of the pure type I fiber population. In contrast, the percentages of type I, type II, and hybrid fibers in the limb muscles (soleus and extensor digitorum longus) did not differ between experimental groups. The optimal length for force production, as well as maximal force-generating capacity of the diaphragm, was also significantly decreased in mechanically ventilated animals. We conclude that even short-term controlled mechanical ventilation produces significant remodeling and functional alterations of the diaphragm, which could impede efforts at discontinuing ventilatory support.

Animals↗
PubMed2002

Gene expression signature of benign prostatic hyperplasia revealed by cDNA microarray analysis.

BACKGROUND: Despite the high prevalence of benign prostatic hyperplasia (BPH) in the aging male, little is known regarding the etiology of this disease. A better understanding of the molecular etiology of BPH would be facilitated by a comprehensive analysis of gene expression patterns that are characteristic of benign growth in the prostate gland. Since genes differentially expressed between BPH and normal prostate tissues are likely to reflect underlying pathogenic mechanisms involved in the development of BPH, we performed comparative gene expression analysis using cDNA microarray technology to identify candidate genes associated with BPH. METHODS: Total RNA was extracted from a set of 9 BPH specimens from men with extensive hyperplasia and a set of 12 histologically normal prostate tissues excised from radical prostatectomy specimens. Each of these 21 RNA samples was labeled with Cy3 in a reverse transcription reaction and cohybridized with a Cy5 labeled common reference sample to a cDNA microarray containing 6,500 human genes. Normalized fluorescent intensity ratios from each hybridization experiment were extracted to represent the relative mRNA abundance for each gene in each sample. Weighted gene and random permutation analyses were performed to generate a subset of genes with statistically significant differences in expression between BPH and normal prostate tissues. Semi-quantitative PCR analysis was performed to validate differential expression. RESULTS: A subset of 76 genes involved in a wide range of cellular functions was identified to be differentially expressed between BPH and normal prostate tissues. Semi-quantitative PCR was performed on 10 genes and 8 were validated. Genes consistently upregulated in BPH when compared to normal prostate tissues included: a restricted set of growth factors and their binding proteins (e.g. IGF-1 and -2, TGF-beta3, BMP5, latent TGF-beta binding protein 1 and -2); hydrolases, proteases, and protease inhibitors (e.g. neuropathy target esterase, MMP2, alpha-2-macroglobulin); stress response enzymes (e.g. COX2, GSTM5); and extracellular matrix molecules (e.g. laminin alpha 4 and beta 1, chondroitin sulfate proteoglycan 2, lumican). Genes consistently expressing less mRNA in BPH than in normal prostate tissues were less commonly observed and included the transcription factor KLF4, thrombospondin 4, nitric oxide synthase 2A, transglutaminase 3, and gastrin releasing peptide. CONCLUSIONS: We identified a diverse set of genes that are potentially related to benign prostatic hyperplasia, including genes both previously implicated in BPH pathogenesis as well as others not previously linked to this disease. Further targeted validation and investigations of these genes at the DNA, mRNA, and protein levels are warranted to determine the clinical relevance and possible therapeutic utility of these genes.

Adult↗
PubMed2002

Alpha-methylacyl-CoA racemase: a new molecular marker for prostate cancer.

Identification of genes that are dysregulated in association with prostate carcinogenesis can provide disease markers and clues relevant to disease etiology. Of particular interest as candidate markers of disease are those genes that are frequently overexpressed. In this study, we describe a gene, alpha-methylacyl-CoA racemase (AMACR), whose expression is consistently up-regulated in prostate cancer. Analysis of mRNA levels of AMACR revealed an average up-regulation of approximately 9 fold in clinical prostate cancer specimens compared with normal. Western blot and immunohistochemical analysis confirms the up-regulation at the protein level and localizes the enzyme predominantly to the peroxisomal compartment of prostate cancer cells. A detailed immunohistochemical analysis of samples from 168 primary prostate cancer cases using both standard slides and tissue microarrays demonstrates that both prostate carcinomas and the presumed precursor lesion (high-grade prostatic intraepithelial neoplasia) consistently scored significantly higher than matched normal prostate epithelium; 88% of the carcinomas had a staining score higher than the highest score observed for any sample of normal prostate epithelium. Both untreated metastases (n = 32 patients) and hormone refractory prostate cancers (n = 14 patients) were generally strongly positive for AMACR. To extend the utility of this marker for prostate cancer diagnosis, we combined staining for cytoplasmic AMACR with staining for the nuclear protein, p63, a basal cell marker in the prostate that is absent in prostate cancer. In a simple assay that can be useful for the diagnosis of prostate cancer on both biopsy and surgical specimens, combined staining for p63 and AMACR resulted in a staining pattern that greatly facilitated the identification of malignant prostate cells. The enzyme encoded by the AMACR gene plays a critical role in peroxisomal beta oxidation of branched chain fatty acid molecules. These observations could have important epidemiological and preventive implications for prostate cancer, as the main sources of branched chain fatty acids are dairy products and beef, the consumption of which has been associated with an increased risk for prostate cancer in multiple studies. On the basis of its consistency and magnitude of cancer cell-specific expression, we propose AMACR as an important new marker of prostate cancer and that its use in combination with p63 staining will form the basis for an improved staining method for the identification of prostate carcinomas. Furthermore, the absence of AMACR staining in the vast majority of normal tissues coupled with its enzymatic activity makes AMACR the ideal candidate for development of molecular probes for the noninvasive identification of prostate cancer by imaging modalities.

Biomarkers, Tumor↗
PubMed2002

Acidic HEPES-KH reperfusion enhances myocardial protection in immature rabbits.

To study the effects of different pH HEPES-KH reperfusate solution on immature myocardial protection, isolated perfused Langendorff model from immature rabbit hearts were developed formed. Control group (C) was perfused only with pH 7.4 HEPES-KH solution for 90 min. Ischemia/reperfusion group (group I/R) was perfused with pH 7.4 HEPES-KH solution before ischemia or after ischemia. Experimental group (group E), after ischemia, was perfused with pH 6.8, pH 7.1 and pH 7.4 HEPES-KH solutions for 5 min, 5 min, and 20 min, respectively. The left ventricular function recovery, MWC, LDH and CK leakage, MDA, ATP content, and SOD activity were determined. Our results showed that the left ventricular function recovery, ATP content and SOD activity in group E were higher than those of group I/R (P < 0.05). MWC, MDA content, LDH and CK leakage in group E were lower than those of group I/R (P < 0.05). These findings suggested that pH paradox might be one of important mechanisms for immature myocardial ischemia-reperfusion injury, and acidic perfusate, at the beginning of reperfusion, might attenuate pH paradox and ameliorate functional recovery in isolated perfused immature rabbit hearts.

Animals↗
PubMed2002

A new lanostane-type triterpene from the fruiting bodies of Ganoderma lucidum.

A new lanostane-type triterpene, named ganoderic acid LM2 (5), was isolated from the fruiting bodies of Ganoderma lucidum. Its structure was characterized as (23S) 7beta, -dihydroxy-3, 11, 15-trioxo-5alpha-lanosta-8, 24-dien-26-oic acid by 1D- and 2D-NMR spectra. In addition, a known triterpene, ganoderic acid epsilon (4), was obtained. Both of them exhibited potent enhancement of ConA-induced mice splenocytes proliferation in vitro.

Animals↗
PubMed2002

[The inhibitory action of the antisense oligodeoxynucleotide to the expression of vascular endothelial growth factor by radiotherapy in a prostate cancer cell line].

OBJECTIVES: To investigate mechanism for the increasing level of serum vascular endothelial growth factor(VEGF) in tumour patients during radiotherapy and the inhibitory action of the antisense oligodeoxynucleotide (AS-ODN) to the expression of VEGF protein by radiotherapy in the prostate cancer cell line (PC3M). METHODS: To observe the changes of serum VEGF in the prostate cancer patients during radiotherapy dynamically and the inhibitory action of the antisense oligodeoxynucleotide to the expression of VEGF by radiotherapy in PC3M. RESULTS: The changes of serum VEGF in three patients receiving radiotherapy had been observed continuously. The levels of serum VEGF began to increase when the patients received radiotherapy and rised up to peak value after fifteen days, then declined to the range of pre-radiotherapy. Irradiating the PC3M cells with X-rays significantly increased the VEGF expression and secretion. The expression of VEGF protein in the group treated by VEGF AS-ODNs and X-ray irradiation decreased significantly than the group treated only by X-ray irradiation. CONCLUSIONS: The induction of VEGF protein expression by X-ray irradiation in tumor cells may result in the increasing of the VEGF in the prostate cancer patients during radiotherapy and the induction can be blocked by VEGF AS-ODNs.

DNA, Antisense↗
PubMed2000

cis-Bis(dicyanamido)bis(1,10-phenanthroline)manganese(II) and cis-bis(dicyanamido)bis(1,10-phenanthroline)zinc(II).

The title compounds are isomorphous, comprised of neutral monomeric [M(phen)(2)(dca)(2)] [(I): M = Mn, (II): M = Zn; phen is 1,10-phenanthroline, C(12)H(8)N(2); dca is dicyanamide, C(2)N(3)] molecules. In the molecule, the divalent metal ion is in a distorted octahedral coordination environment formed by six N atoms from the phen and dca ligands. The Mn-N [2.144 (2)-2.319 (2) A] and Zn-N [2.075 (2)-2.245 (2) A] distances are in agreement with the difference in size of the two divalent ions.

Journal Article↗
PubMedDate not supplied

Effects of three-dimensional culturing in a fibrous matrix on cell cycle, apoptosis, and MAb production by hybridoma cells.

The effects of culturing hybridoma cells in a three-dimensional (3-D) poly(ethylene terephthalate) (PET) fibrous matrix on cell cycle, apoptosis, metabolism, and monoclonal antibody (MAb) production were evaluated by comparing with two-dimensional (2-D) culturing on microcarrier and multiwell plate surfaces. The percentage of cells in the G1/G0 phase increased during the long-term culturing period of approximately 4 weeks. Compared to the 2-D culture systems, cells grown in 3-D matrices had higher MAb productivity for long-term culture. Decreasing serum content in the culture medium increased both MAb productivity and apoptosis. However, the 3-D culture had a greater increase in MAb productivity and a much lower apoptotic rate than the 2-D culture, especially at 0% serum. Most cells in the 3-D fibrous matrix formed large aggregates and were smaller than cells grown on a 2-D surface or in suspension. The smaller cell size allowed cells to survive better in the high-cell-density environment. The fibrous matrix also selectively retained healthy, nonapoptotic cells. These results suggested that the 3-D fibrous matrix contributed to growth arrest, protected cells to better resist low-serum environments, and reduced apoptosis, all of which contributed to the high viable cell density and volumetric MAb productivity in the long-term 3-D culture.

Animals↗
PubMedDate not supplied

Inactivation of primary antioxidant enzymes in mouse keratinocytes by photodynamically generated singlet oxygen.

Cellular antioxidant enzymes protect against damage caused by exposure to endogenous or exogenous prooxidants. Singlet oxygen ((1)O(2)) is a reactive form of oxygen that can be produced in vivo either in normal and pathophysiologic conditions or by photosensitizing chemicals, as during photodynamic treatment. We hypothesized that photodynamically generated (1)O(2) would decrease the enzymatic activities of cellular antioxidants. To test this hypothesis, we treated cultured mouse epidermal keratinocytes with the photosensitizer Photofrin plus visible light to produce (1)O(2), and then measured CuZnSOD, MnSOD, and catalase activities with both ingel and spectrophotometric enzyme activity assays. Our results demonstrated that the enzymatic activities of cellular CuZnSOD, MnSOD, and catalase were significantly decreased after keratinocytes were treated with Photofrin plus visible light. By contrast, the enzymatic activities of cellular CuZnSOD, MnSOD, and catalase were unaffected in control cells treated with Photofrin only or visible light only. Despite the decreased levels of enzymatic activities, the protein levels of all three primary antioxidant enzymes remained constant after photodynamic treatment, as determined by Western blotting. L-Histidine, a (1)O(2) quencher, protected against the inactivation of cellular CuZnSOD, MnSOD, and catalase enzymes induced by photodynamically generated (1)O(2). The conclusion from these experiments is that the primary cellular antioxidant enzymes CuZnSOD, MnSOD, and catalase can be inactivated by photodynamically generated (1)O(2) in nucleated mammalian cells. These findings may be useful in the future development of antineoplastic adjuvant therapies that use photodynamic generation of (1)O(2) to inactivate antioxidant defenses with a goal of sensitizing tumor cells to prooxidant-generating drugs.

Animals↗